Regional Temperature Changes in the Brain during Somatosensory Stimulation

Trübel, H.; Sacolick, Laura; Hyder, Fahmeed

doi:10.1038/sj.jcbfm.9600164

Cited by 59 publications

(63 citation statements)

References 72 publications

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“…The simulated BOLD data were generated with a step size of 0.1s using the Metabolic/Hemodynamic Model (MHM) proposed in Sotero and Trujillo-Barreto (2007) with the standard parameters set used in that paper. While the time characterizing BOLD changes in the brain is in the order of seconds, in the case of temperature changes is in the order of minutes (Trübel et al, 2006). This explains why while there is no interaction between the multiples BOLD responses in Figure 1 and Figure 2, there is at the resulting temperature signals.…”

Section: From Simulated Bold Data To Temperature Time Seriesmentioning

confidence: 96%

“…when the resting state is disturbed by global changes in blood flow, incoming blood temperature, or oxygen consumption (Pennes, 1948;Yablonskiy et al, 2000;Trübel et al, 2006): Table 1.…”

Section: Modelling Temperature Changesmentioning

confidence: 99%

“…The second term is the rate of heat removal from brain tissue by cerebral blood flow, and the third term describes conductive heat loss within brain tissue (Trübel et al, 2006). By substituting 0 T = ɺ in (1) we found the temperature at rest ( )…”

Section: Modelling Temperature Changesmentioning

confidence: 99%

“…The balance between metabolic heat production (due to the oxidation of glucose), heat removal by cerebral blood flow ( ) CBF , and conductive heat loss from the region of interest (ROI) to neighbouring regions, characterize the temperature dynamics in the ROI (Trübel et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Thus, it has been proposed (Yablonskiy et al, 2000) that disproportional changes in cerebral metabolic rate of oxygen consumption ( ) 2 CMRO and CBF evoked by neuronal activity can explain the variation in brain tissue temperature (in the range of 0 0.2 C ± ) revealed by functional studies in humans (Yablonskiy et al, 2000;Shevelev et al, 1993;Gorbach et al, 2003) and animals (Trübel et al, 2006;Serota and Gerard, 1938;McElligot and Melzack, 1967;Melzack and Casey, 1967;Hayward and Baker, 1968;LaManna et al, 1989;Gorbach, 1993;Shevelev and Tsicalov, 1997;Shevelev, 1998).…”

Section: Introductionmentioning

confidence: 99%

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From Blood Oxygenation Level Dependent (BOLD) Signals to Brain Temperature Maps

Sotero

Iturria-Medina

2011

Bull Math Biol

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A theoretical framework is presented for converting Blood Oxygenation Level Dependent (BOLD) images to temperature maps, based on the idea that disproportional local changes in cerebral blood flow (CBF) as compared with cerebral metabolic rate of oxygen consumption (CMRO 2 ) during functional brain activity, lead to both brain temperature changes and the BOLD effect. Using an oxygen limitation model and a BOLD signal model we obtain a transcendental equation relating CBF and CMRO 2 changes with the corresponding BOLD signal, which is solved in terms of the Lambert W function. Inserting this result in the dynamic bio-heat equation describing the rate of temperature changes in the brain, we obtain a non autonomous ordinary differential equation that depends on the BOLD response, which is solved numerically for each brain voxel. In order to test the method, temperature maps obtained from a real BOLD dataset are calculated showing temperature variations in the range: (-0.15, 0.1) which is consistent with experimental results. The method could find potential clinical uses as it is an improvement over conventional methods which require invasive probes and can record only few locations simultaneously. Interestingly, the statistical analysis revealed that significant temperature variations are more localized than BOLD activations. This seems to exclude the use of temperature maps for mapping neuronal activity as areas where it is well known that electrical activity occurs (such as V5 bilaterally) are not activated in the obtained maps. But it also opens questions about the nature of the information processing and the underlying vascular network in visual areas that give rise to this result.

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Section: From Simulated Bold Data To Temperature Time Seriesmentioning

confidence: 96%

“…when the resting state is disturbed by global changes in blood flow, incoming blood temperature, or oxygen consumption (Pennes, 1948;Yablonskiy et al, 2000;Trübel et al, 2006): Table 1.…”

Section: Modelling Temperature Changesmentioning

confidence: 99%

Section: Modelling Temperature Changesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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From Blood Oxygenation Level Dependent (BOLD) Signals to Brain Temperature Maps

Sotero

Iturria-Medina

2011

Bull Math Biol

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Sources of phase changes in BOLD and CBV‐weighted fMRI

Zhao

Jin

Wang

et al. 2007

Magnetic Resonance in Med

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Phase changes in blood oxygenation-level dependent (BOLD) fMRI have been observed in humans; however, their exact origin has not yet been fully elucidated. To investigate this issue, we acquired gradient-echo (GE) BOLD and cerebral blood volume (CBV)-weighted fMRI data in anesthetized cats during visual stimulation at 4.7T and 9.4T, before and after injection of a superparamagnetic contrast agent (monocrystalline iron oxide nanoparticles, MION), respectively. In BOLD fMRI, large positive changes in both magnitude and phase were observed predominantly in the cortical surface area, where the large draining veins reside. In CBV-weighted fMRI, large negative changes in both magnitude and phase were detected mainly in the middle cortical area, where the greatest CBV change takes place. Additionally, the phase change was temporally correlated with the magnitude response and was linearly dependent on the echo time (TE), which cannot be explained by the intravascular (IV) contribution and functional temperature change. Phase changes with the opposite polarity were also observed in the regions around the dominant phase changes. These phase Functional magnetic resonance imaging (fMRI) based on blood oxygenation level-dependent (BOLD) (1-3) signal has become a routine tool for studying the brain, particularly in human subjects. As an alternative to BOLD, cerebral blood volume (CBV)-weighted fMRI can be performed with the use of superparamagnetic exogenous intravascular (IV) contrast agents, such as monocrystalline iron oxide nanoparticles (MION), in animal models (4 -7). The physical source of both the BOLD and the CBV-weighted fMRI signals is the change in field inhomogeneity generated by the magnetic susceptibility effect in blood due to paramagnetic deoxyhemoglobin or exogenous contrast agents (1). During brain activation, changes in deoxyhemoglobin and blood volume modulate the field inhomogeneity inside and outside blood vessels and thus the spins' coherence, which in turn alters the magnitude of the MRI signal.The susceptibility effects of blood vessels can be approximately modeled as infinite cylinders (8,9). The resonance frequency of a water proton is shifted from the Larmor frequency due to the susceptibility difference between blood and tissue water. For extravascular (EV) water, the magnetic field change (⌬B) is a sum of magnetic field changes induced by all blood vessels that exhibit magnetic perturbations, and can be written as:where ⌬ is the susceptibility difference between IV blood and surrounding tissue, R is the vessel radius, r is the distance between the point of interest and the center of the vessel in the plane through the point of interest and perpendicular to the vessel, is the angle between the main magnetic field B 0 and the vessel orientation, and is the angle between position vector r in this plane and the projection of B 0 in the plane. When the frequency shift induced by ⌬B is integrated around vessels (i.e., ranges from 0°to 360°), the average frequency shift for all the protons in an imagin...

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Interleukin‐1 exacerbates focal cerebral ischemia and reduces ischemic brain temperature in the rat

Parry‐Jones

Liimatainen

Kauppinen

et al. 2008

Magnetic Resonance in Med

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The proinflammatory cytokine interleukin-1 (IL-1) is a key mediator of inflammation in cerebral ischemia, but its precise mechanisms of action remain elusive. Temperature is critical to outcome in brain injury and given the importance of IL-1 in pyrogenesis this has clear mechanistic implications. IL-1 exacerbates ischemia independently of core (rectal) temperature. However, it is temperature in the ischemic brain that influences outcome and rectal temperature is likely to be a poor surrogate marker. This study tested the hypothesis that IL-1 exacerbates cerebral ischemia by increasing ischemic brain temperature. Wistar rats undergoing transient middle cerebral artery occlusion received either 4 g/kg IL-1 (n ‫؍‬ 9) or vehicle (n ‫؍‬ 10) intraperitoneally. NMR-generated maps of brain temperature, tissue perfusion, and the trace of the diffusion tensor were collected during occlusion, early reperfusion, and at 24 hr. IL-1 significantly increased ischemic damage at 24 hr by 35% but rectal temperature did not vary significantly between groups. However, ischemic brain was 1.7°C cooler on reperfusion in IL-1-treated animals (vs. vehicle) and a corresponding reduction in cerebral blood flow was identified in the ischemic striatum. Contrary to the stated hypothesis, IL-1 reduced ischemic brain temperature during reperfusion and this may be due to a reduction in tissue perfusion.

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Regional Temperature Changes in the Brain during Somatosensory Stimulation

Cited by 59 publications

References 72 publications

From Blood Oxygenation Level Dependent (BOLD) Signals to Brain Temperature Maps

From Blood Oxygenation Level Dependent (BOLD) Signals to Brain Temperature Maps

Sources of phase changes in BOLD and CBV‐weighted fMRI

Interleukin‐1 exacerbates focal cerebral ischemia and reduces ischemic brain temperature in the rat

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